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61.
目的 评价二氧化碳(C02)气腹对腹腔镜手术患者顺阿曲库铵肌松效应的影响.方法 择期子宫切除术患者60例,年龄35 ~ 60岁,BMI 18~ 24 kg/m2,ASA分级Ⅰ或Ⅱ级.采用随机数字表法,将其随机分为2组(n=30):气腹组(P组)和对照组(C组);每组根据肌松拮抗剂使用情况随机分为2个亚组(n=15):非拮抗组(P0组或C0组)和拮抗组(P1组或C1组).静脉注射芬太尼、丙泊酚、顺阿曲库铵麻醉诱导,气管插管后行机械通气.靶控输注丙泊酚和瑞芬太尼维持麻醉.采用TOF-Watch SX加速度仪监测肌松程度,P组于气腹建立后T1恢复达5%时静脉注射顺阿曲库铵0.05mg/kg,术毕P1组和C1组于 T1恢复至25%时静脉注射新斯的明拮抗,P0组和C0组自然恢复.记录气腹建立后追加顺阿曲库铵的临床作用时间和恢复指数.于诱导前即刻、气腹30 min、60 min及术毕时,分别抽取动脉血样行血 气分析.结果 与C0组比较,P0组临床作用时间及恢复指数延长(P<0.05);与C1组比较,P1组临床作用时间及拮抗恢复指数延长(P<0.05);与 C0组比较,P0组于气腹30、60 min、术毕时pH值下降,PaCO2升高(P<0.05);与C1组比较,P1组于气腹30、60 min、术毕时pH值下降,PaCO2升高(P<0.05).结论 CO2气腹可强化顺阿曲库铵的肌松效应,且可延长拮抗后肌松恢复时间.  相似文献   
62.
目的 比较不同剂量顺式阿曲库铵对患者拇内收肌与眼轮匝肌的肌松效应.方法 全麻患者25例,ASA Ⅰ或Ⅱ级,年龄42~64岁,体重51~81 kg,随机分为2组,顺式阿曲库铵0.075ms/ks组(Ⅰ组,n=11)和顺式阿曲库铵0.15 mg/kg组(Ⅱ组,n=14).静脉注射咪达唑仑0.035~0.045mg/kg、异丙酚1.5~2 mg/kg、芬太尼0.1~0.2 mg、顺式阿曲库铵0.075 mg/kg或0.15 mg/kg行麻醉诱导,吸入50%氧化亚氮、间断静脉注射芬太尼维持麻醉.采用2台TOF-Watch SX加速度肌松监测仪同步监测眼轮匝肌和拇内收肌的神经肌肉阻滞情况,记录肌松起效时间、无反应期及T25%和T75%恢复时间.于眼轮匝肌肌颤搐抑制75%~80%时行气管插管,并评价气管插管条件.结果 2组气管插管条件良好且差异无统计学意义(P>0.05);与Ⅰ组比较,Ⅱ组拇内收肌和眼轮匝肌肌松起效时间缩短,T25%恢复时间、T75%恢复时间和无反应期延长(P<0.01);与拇内收肌比较,Ⅰ组眼轮匝肌T75%恢复时间缩短,Ⅱ组眼轮匝肌无反应期和T25%恢复时间缩短(P<0.05或0.01).结论 顺式阿曲库铵对拇内收肌和眼轮匝肌的肌松效应呈剂量依赖性,眼轮匝肌对顺式阿曲库铵的敏感性低于拇内收肌;监测顺式阿曲库铵对眼轮匝肌神经肌肉阻滞情况可有效指导气管插管.  相似文献   
63.
阿曲可林和维库溴铵间歇静注法和持续静滴法的比较研究   总被引:1,自引:1,他引:0  
本文在80例颅脑胸腹部等手术病人,通过TOF监测神经肌接头功能,观察阿曲可林和维库溴铵间歇静注和持续静滴两种给药方法的肌松程度、用药量和恢复时间。结果:(1)间歇静注需频繁给药,肌松程度波动较大,持续静滴法肌松程度恒定。(2)维持肌颤搐25%以下的静注法与维持肌颤搐5-10%的静滴法的用药量几乎相等,阿曲可林为6.05~6.71μg/kg/min,维库溴铵为1.11~1.12μg/kg/min。(  相似文献   
64.
顺阿曲库铵的药效学及其对组胺释放的影响   总被引:1,自引:0,他引:1  
目的 比较全麻诱导期间不同保存条件下顺阿曲库铵和阿曲库铵的药效学及其对组胺释放的影响.方法 择期全麻手术患者45例,ASA Ⅰ或Ⅱ级,年龄16-71岁,随机分为3组(n=15):阿曲库铵冷藏组(ATR冷藏组)、顺阿曲库铵冷藏组(CIS冷藏组)和顺阿曲库铵常温组(CIS常温组).靶控输注异丙酚血浆靶浓度3μg/ml和瑞芬太尼效应室靶浓度3~5 ng/ml行麻醉诱导.ATR冷藏组静脉注射冷藏保存的阿曲库铵0.75 mg/kg,CIS冷藏组和CIS常温组分别静脉注射冷藏或室温保存的顺阿曲库铵0.15 mg/kg.使用肌松监测仪,采用单次颤搐刺激(频率0.1Hz,刺激持续时间0.2ms),测定刺激前臂尺神经拇内收肌的加速度.记录肌颤搐最大抑制程度、起效时间、作用时间和恢复指数.肌颤搐抑制达最大抑制时行气管插管,机械通气,评价气管插管条件.于麻醉诱导前(T0)、给予静脉全麻药后2min(T1)、给予肌松药后2min(T2)和5min(T3)时,记录MAP和HR,观察皮肤情况,同时采集桡动脉血样2ml,采用酶联免疫吸附法测定血浆组胺浓度.结果 CIS冷藏组和ATR冷藏组肌颤搐抑制均可达100%,CIS常温组仅53.33%的患者肌颤搐抑制最大达90%.与ATR冷藏组比较,CIS冷藏组起效时间延长,作用时间缩短(P<0.05),恢复指数差异无统计学意义(P>0.05);与CIS冷藏组比较,CIS常温组起效时间延长,作用时间缩短(P<0.05),恢复指数差异无统计学意义(P>0.05).ATR冷藏组和CIS冷藏组的气管插管条件优于CIS常温组(P<0.05).两组间不同时点血浆组胺浓度、MAP和HR比较差异无统计学意义(P>0.05);与T0时比较,ATR冷藏组T2,3时血浆组胺浓度升高,T1~3时MAP降低,CIS冷藏组T1~3时MAP降低(P<0.05).各组患者皮肤均未发现任何变化.结论 与冷藏保存的阿曲库铵相比,冷藏保存的顺阿曲库铵肌松作用强而起效较慢,作用时间较短,不引起组胺释放,可安全地应用于全身麻醉.但该药在室温下保存120d后,药效稳定性较差.  相似文献   
65.
目的探讨阿曲库铵协同简易呼吸机在危重患者转运中的作用。方法对50例危重合并呼吸衰竭病人院前急救途中使用阿曲库铵联合简易呼吸机治疗效果进行观察与分析。结果使用阿曲库铵协同简易呼吸机使50例危重患者的呼吸困难症状明显改善,动脉血氧饱和度≥92%。全部病例在转运或送检CT检查情况时无1例死亡。结论院前急救转运途中对呼吸衰竭的危重患者使用简易呼吸机施行控制呼吸,改善患者呼吸困难、提高血氧饱和度效果明显。是一种安全可行的方法,值得在临床推广使用。  相似文献   
66.
卡肌宁前处理对琥珀胆碱Ⅱ相阻滞的影响   总被引:1,自引:0,他引:1  
研究卡肌宁前处理对长时间反复静注琥珀胆碱效应的影响。结果:前处理对单次静注琥珀胆碱的起效时间、作者持续时间和恢复时间无明显影响。但牟显著地降低由琥珀胆碱引起的肌颤增强现象;对长时间反复静注琥珀胆碱能明显地延缓Ⅱ相阻滞的发生时间,提高神经肌肉的自然恢复率。由此可见,卡肌宁为一种良好的前处理药物。  相似文献   
67.
68.
BACKGROUND: Neuromuscular blocking agents may exert central nervous system effects when they reach the brain. This study assessed the concentrations and the time course of passage of vecuronium, atracurium, and its metabolite laudanosine in the cerebrospinal fluid (CSF) of patients undergoing intracranial aneurysm clipping. METHODS: Twenty-five patients with subarachnoid hemorrhage were randomly allocated to receive an intravenous infusion of vecuronium (n=13) or atracurium (n=12). Arterial blood and lumbar CSF were sampled before and 1, 2, 3, 4 and 8 h after the start of the relaxant infusion. The samples were analyzed by liquid chromatography-electrospray ionization mass spectrometry (vecuronium) and high-pressure liquid chromatography (atracurium and laudanosine). RESULTS: The data of 20 patients (10 in both groups) were analyzed. In 11 CSF samples from five patients atracurium was detected in concentrations from 10 to 50 ng/ml. Laudanosine was retrieved in all CSF samples at 1, 2, 3, 4 and 8 h; the highest CSF concentration of laudanosine occurred at 3 h [38 (18-63) ng/ml: median (range)]. Vecuronium was not found in any CSF sample. CONCLUSION: Significant concentrations of atracurium and laudanosine but not of vecuronium were detected in the CSF of patients during and immediately after intracranial aneurysm surgery.  相似文献   
69.
Glioblastoma multiforme (GBM) are the most common primary malignant brain tumor in adults, with a median survival of about one year. This poor prognosis is attributed primarily to therapeutic resistance and tumor recurrence after surgical removal, with the root cause suggested to be found in glioblastoma stem cells (GSCs). Using glial fibrillary acidic protein (GFAP) as a reporter of astrocytic differentiation, we isolated multiple clones from three independent GSC lines which express GFAP in a remarkably stable fashion. We next show that elevated expression of GFAP is associated with reduced clonogenicity in vitro and tumorigenicity in vivo. Utilizing this in vitro cell-based differentiation reporter system we screened chemical libraries and identified the non-depolarizing neuromuscular blocker (NNMB), Atracurium Besylate, as a small molecule which effectively induces astroglial but not neuronal differentiation of GSCs. Functionally, Atracurium Besylate treatment significantly inhibited the clonogenic capacity of several independent patient-derived GSC neurosphere lines, a phenomenon which was largely irreversible. A second NNMB, Vecuronium, also induced GSC astrocytic differentiation while Dimethylphenylpiperazinium (DMPP), a nicotinic acetylcholine receptor (nAChR) agonist, significantly blocked Atracurium Besylate pro-differentiation activity. To investigate the clinical importance of nAChRs in gliomas, we examined clinical outcomes and found that glioma patients with tumors overexpressing CHRNA1 or CHRNA9 (encoding for the AChR-α1 or AChR-α9) exhibit significant shorter overall survival. Finally, we found that ex-vivo pre-treatment of GSCs, expressing CHRNA1 and CHRNA9, with Atracurium Besylate significantly increased the survival of mice xenotransplanted with these cells, therefore suggesting that tumor initiating subpopulations have been reduced.  相似文献   
70.
IntroductionThe association between Local Anesthetics (LAs) and Neuromuscular Blocking (NMB) drugs in clinical practice, and the possibility of interaction between these drugs has been investigated. LAs act on neuromuscular transmission in a dose‐dependent manner and may potentiate the effects of NMB drugs.ObjectiveThe aim of this study was to evaluate, in an experimental model, the effect of lidocaine and racemic bupivacaine on neuromuscular transmission and the influence on neuromuscular blockade produced by atracurium.MethodsMale Wistar rats, weighing from 250 g to 300 g were used. The preparation was set up based on a technique proposed by Bülbring. Groups were formed (n = 5) according to the drug studied: lidocaine 20 μg.mL‐1 (Group I); racemic bupivacaine 5 μg.mL‐1 (Group II); atracurium 20 μg.mL‐1 (Group III); atracurium 20 μg.mL‐1 in a preparation previously exposed to lidocaine 20 μg.mL‐1 and racemic bupivacaine 5 μg.mL‐1, Groups IV and V, respectively. The following parameters were assessed: 1) Amplitude of hemi diaphragmatic response to indirect stimulation before and 60 minutes after addition of the drugs; 2) Membrane Potentials (MP) and Miniature Endplate Potentials (MEPPs).ResultsLidocaine and racemic bupivacaine alone did not alter the amplitude of muscle response. With previous use of lidocaine and racemic bupivacaine, the neuromuscular blockade (%) induced by atracurium was 86.66 ± 12.48 and 100, respectively, with a significant difference (p = 0.003), in comparison to the blockade produced by atracurium alone (55.7 ± 11.22). These drugs did not alter membrane potential. Lidocaine initially increased the frequency of MEPPs, followed by blockade. With the use of bupivacaine, the blockade was progressive.ConclusionsLidocaine and racemic bupivacaine had a presynaptic effect expressed by alterations in MEPPs, which may explain the interaction and potentiation of NMB produced by atracurium.  相似文献   
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